Basics

Description

Clinical symptoms are often secondary to small vessel occlusion or a hyperviscosity syndrome in type I CGs or the formation of CG-containing immune complexes leading to vasculitis in type II and type III CGs.

Etiology and Pathophysiology

Exact mechanism of cold insolubility in these cryoproteins is unknown. Hypotheses include reduced concentrations of sialic acid and galactose in the Fc region of Ig as well as steric conformation changes due to temperature variation.

Basics

Description

Clinical symptoms are often secondary to small vessel occlusion or a hyperviscosity syndrome in type I CGs or the formation of CG-containing immune complexes leading to vasculitis in type II and type III CGs.

Etiology and Pathophysiology

Exact mechanism of cold insolubility in these cryoproteins is unknown. Hypotheses include reduced concentrations of sialic acid and galactose in the Fc region of Ig as well as steric conformation changes due to temperature variation.